Air entry was present on the right side with no adventitious sounds. Endotracheal suction was done to rule out the blockage of ETT. However, EtCO 2 continued to rise till 113–115 mm Hg. EtCO 2 reached up to 60 mmHg after which we started manually ventilating the patient. After CO 2 insufflation in the thorax, there was rise in the EtCO 2 and the inspiratory pressure requirement. The patient was given right lateral position and was ventilated using pressure control mode achieving tidal volume of 6 ml/kg. The absence of air entry on the operative left side was confirmed by auscultation.

Right endobronchial intubation was done with 4.5 mm ID endotracheal tube (ETT). After premedication, anaesthesia was induced with sevoflurane and injection Atracurium 0.6 mg/kg. All other investigations were within normal limits. The air entry was diminished on the left side. Computed tomography scan showed a 31 mm × 28 mm × 38 mm fluid density lesion seen in posterior mediastinum causing severe compression of the left main bronchus with resultant obstructive emphysema. The patient had a history of fever and cough on and off for 1 year. We encountered a similar situation in a 2 year old child weighing 10 kg posted for thoracoscopic excision of a left bronchogenic cyst. Reversal of the normally positive PaCO 2-EtCO 2 gradient may occur also termed as negative arterial to EtCO 2 gradient. However, in conditions where there is ventilation-perfusion mismatch, the EtCO 2 may not accurately reflect the PaCO 2. The PaCO 2 is normally higher than EtCO 2 by 2-5 mmHg.

End-tidal CO 2 (EtCO 2) is used as a surrogate to assess adequacy of ventilation since it provides an estimate of the arterial CO 2 (PaCO 2).

Endtidal co2